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Rictor regulates cell migration by suppressing RhoGDI2

N K Agarwal1, C-H Chen, H Cho

  • 1Department of Molecular and Cellular Oncology, University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.

Oncogene
|July 11, 2012
PubMed

Insights

Rictor protein suppresses RhoGDI2, enhancing Rho protein activity and promoting cell migration. This finding clarifies rictor

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Biochemistry

Background:

  • Rictor is a key component of mTORC2, a signaling complex regulating AGC kinases involved in cell proliferation and survival.
  • Rictor's ortholog in Dictyostelium regulates cell migration, but the underlying mechanisms are not well understood.

Purpose of the Study:

  • To elucidate the mechanism by which rictor regulates cell migration.
  • To investigate the role of rictor in controlling Rho protein activity.

Main Methods:

  • Proteomics analysis to identify rictor-dependent changes in protein expression.
  • Investigation of Rho-GDP dissociation inhibitor 2 (RhoGDI2) levels and activity of Rho proteins (Rac and Cdc42).
  • Functional assays to assess cell migration.

Main Results:

  • Rictor deficiency leads to increased RhoGDI2, which inhibits Rho protein activity (Rac and Cdc42) and impairs cell migration.
  • Rictor directly suppresses RhoGDI2, independent of Sin1 (mTORC2) or raptor (mTORC1) function.
  • Suppression of RhoGDI2 by rictor is crucial for promoting Rho protein activity and facilitating cell migration.

Conclusions:

  • Rictor regulates cell migration by controlling RhoGDI2 levels.
  • Rictor's suppression of RhoGDI2 enhances Rho protein activity, thereby promoting cell migration.
  • This mechanism highlights a novel role for rictor in cytoskeletal dynamics and cell motility.

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